1. INFLAMMATORY & VALVULAR HEART DISEASE

2. Objectives
Compare and contrast inflammatory and valvular heart disease
Evaluate a comprehensive plan of care for the client with inflammatory and valvular heart disease.

3. Layers of the Heart
Fig Layers of the heart muscle and pericardium. The section of the heart wall shows the fibrous pericardium, the parietal and visceral layers of the serous pericardium (with the pericardial sac between them), the myocardium, and the endocardium.

4. Inflammatory Heart Disease
Infective Endocarditis
Pericarditis
Rheumatic Fever
Myocarditis

5. Infective Endocarditis
Infection of the inner layer of the heart that usually affects the cardiac valves
Almost always a fatal condition until development of penicillin
15,000 new cases diagnosed in the United States each year
Subacute form
Preexisting valve disease
Longer clinical course
Insidious onset
Caused by enterococci
Acute form
Healthy valves
Shorter clinical course
Rapid onset

6. Etiology & Pathophysiology
Occurs when blood turbulence within heart allows causative agent to infect previously damaged valves or other endothelial surfaces

7. Cont’d Principal risk factors Age Intravenous drug abuse (IVDA)
Prosthetic valves
Use of intravascular devices
Renal dialysis

8. Cont’d Vegetation Fibrin, leukocytes, platelets, and microbes
Adhere to the valve or endocardium
Embolization of portions of vegetation into circulation

9. Fig. 37-2. Bacterial endocarditis of the mitral valve
Fig Bacterial endocarditis of the mitral valve. The valve is covered with large, irregular vegetations (arrow).

10. Causes
Streptococcus viridans
Staphylococcus aureus
Viruses
Fungi

11. Clinical Manifestation
Nonspecific
Fever occurs in 90% of patients.
Chills
Weakness
Malaise
Fatigue
Anorexia
Murmur
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Subacute form
Arthralgias
Myalgias
Back pain
Abdominal discomfort
Weight loss
Headache
Clubbing of fingers
Vascular manifestations
Splinter hemorrhages in nail beds
Petechiae
Osler’s nodes on fingers or toes
Janeway’s lesions on palms or soles
Roth’s spots
Murmur in most patientsThe onset of a new or changing murmur is noted in most patients with IE, with the aortic and mitral valves most commonly affected. Murmurs are often absent in tricuspid endocarditis because right-sided heart pressures are too low to be heard.
Heart failure in up to 80% with aortic valve endocarditis
Manifestations secondary to embolism
Clinical manifestations secondary to embolization in various body organs may also be present. Organs involved may be the spleen, kidney, peripheral blood vessels of the arm and leg, brain, and lung.

12. Diagnosis Thorough H&P Dental Procedures Invasive Procedures
IV devices
Other recent infections
Labwork & Dx Studies
History
Recent dental, urologic, surgical, or gynecologic procedures
Heart disease
Recent cardiac catheterization or surgery
Intravascular device placement
Renal dialysis
Skin, respiratory, or urinary tract infection
Laboratory tests
Blood cultures
WBC with differential
Echocardiography
Chest x-ray
Two blood cultures drawn 30 minutes apart from two different sites will be positive in more than 90% of patients.
A mild leukocytosis occurs in acute endocarditis (uncommon in subacute), with average white blood cell (WBC) counts ranging from 10,000 to 11,000 μL (10 to 11 × 109/L). Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels may be elevated.
Echocardiography is valuable in the diagnostic workup for a patient with IE when the blood cultures are negative, or for the patient who is a surgical candidate and has an active infection.
A chest x-ray examination is done to detect the presence of cardiomegaly (an enlarged heart).

13. Collaborative Care
What could be done for patients having procedures involving:
Certain dental procedures
Respiratory tract incisions
GI wound infection
Urinary tract infection
___________________________________ ___??
Antibiotic administration
Monitor antibiotic serum levels (e.g., peak and trough).
Subsequent blood cultures
Monitor renal function.
Accurate identification of the infecting organism is the key to successful treatment of IE. Long-term treatment is necessary to kill dormant bacteria clustered within the valvular vegetations. Complete eradication of the organism generally takes weeks to achieve, and relapses are common.

14. Acute Pericarditis
Inflammation of the pericardium, the membranous sac enveloping the heart.
It may be a primary illness or it may develop during various medical and surgical disorders.
Asymptomatic or chest pain/friction rub
Motrin/bedrest/maybe pericardiocentesis/watch for cardiac tamponade

15. Myocarditis Inflammatory process involving the myocardium
Results from infection, usually asymptomatic
Frequently associated with acute pericarditis
Treat underlying cause

16. Rheumatic Fever
Inflammatory disease of the heart potentially involving all layers of the heart
RHEUMATIC HEART DISEASE:
Chronic condition resulting from rheumatic fever, charachterized by scarring and deformity of the heart valves

17. Valve Disorders Regurgitation (re-GUR-jih-TA- shun)
Stenosis (ste-NO-sis)
When valves do not close completely, blood flows backward through the valve in a process called regurgitation.
When valves do not open completely, a condition called stenosis, the flow of blood through the valve is reduced.
Atresia occurs if a heart valve lacks an opening for blood to pass through.
Stenosis
Valve orifice is restricted.
Forward blood flow is impeded.
A pressure gradient is created across open valve.
Pressure gradient differences reflect the degree of stenosis.
Regurgitation
Incomplete closure of valve leaflets
Results in backward flow of blood
Valvular disorders occur in children and adolescents primarily from congenital conditions and in adults from some form of cardiovascular disease.

18. Valve Dysfunction
When any of the heart valves do not close or open properly, blood flow is affected.
How the Heart Works:
Tricuspid valve, separates the right atrium from the right ventricle,
Mitral valve, which separates the left atrium from the left ventricle.
Tricuspid valve has three leaflets; the mitral valve has two.
Both valves have chordae tendineae that anchor the valve leaflets to the papillary muscles and ventricular wall.
Semilunar valves are located between the ventricles and their corresponding arteries.
The pulmonic valve lies between the right ventricle and the pulmonary artery
The aortic valve lies between the left ventricle and the aorta.

19. Normal Heart

20. Valvular Stenosis and Regurgitation
Fig Valvular stenosis and regurgitation. A, Normal position of the valve leaflets, or cusps, when the
valve is open and closed. B, Open position of a stenosed valve (left) and position of closed regurgitant valve
(right). C, Hemodynamic effect of mitral stenosis. The stenosed valve is unable to open sufficiently during left
atrial systole, inhibiting left ventricular filling. D, Hemodynamic effect of mitral regurgitation. The mitral valve
does not close completely during left ventricular systole, permitting blood to reenter the left atrium.

21. Mitral Valve Stenosis
Rheumatic mitral stenosis is widespread in developing countries.
Less common causes are congenital mitral stenosis, rheumatoid arthritis, and systemic lupus erythematosus.
Majority of adult cases result from rheumatic heart disease.
Causes scarring of valve leaflets and chordae tendineae
Contractures develop with adhesions between commissures of the leaflets.
Stenotic mitral valve assumes “fish mouth” shape caused by thickening and shortening of valve strictures.
Result = Obstruction
↑ left atrial pressure and volume
Hypertrophy of pulmonary vessels
Chronic left atrial pressure elevations
Mitral stenosis is an obstruction of blood flowing from the left atrium into the left ventricle.
It is most often caused by rheumatic endocarditis, which progressively thickens the mitral valve leaflets and chordae tendineae.
The leaflets often fuse together.
Eventually, the mitral valve orifice narrows and progressively obstructs blood flow into the ventricle.
The opening narrows to the width of a pencil.
The left atrium has great difficulty moving blood into the ventricle because of the increased resistance of the narrowed orifice.
The left atrium dilates (stretches) and hypertrophies (thickens) because of the increased blood volume it holds.
Because there is no valve to protect the pulmonary veins from the backward flow of blood from the atrium, the pulmonary circulation becomes congested.
As a result, the right ventricle must contract against an abnormally high pulmonary arterial pressure and is subjected to excessive strain.
Eventually, the right ventricle fails.
The enlarged left atrium may create pressure on the left bronchial tree, resulting in a dry cough or wheezing
Difficulty breathing
Fatigue
Low cardiac output
Hemoptysis
Cough; wheeze
Experience palpitations, orthopnea, paroxysmal nocturnal dyspnea (PND), and repeated respiratory infections.
Pulse is weak and often irregular because of atrial fibrillation (caused by the strain on the atrium).
A low-pitched, rumbling, diastolic murmur is heard at the apex.
As a result of the increased blood volume and pressure, the atrium dilates, hypertrophies, and becomes electrically unstable, and patients experience atrial dysrhythmias.
Echo, cath, CHF pt’s treated accordingly
Anticoagulants to avoid thrombosis
Antibiotics to prevent infective endocarditis
Avoid strenuous activity

22. Mitral Valve Regurgitation
Valve patency depends on
Left atrium
Left ventricle
Abnormality of any of these structures can result in regurgitation.
Majority of cases attributed to MI
Chronic rheumatic heart disease
Mitral valve prolapse
Acute: A low CO may mask a new systolic murmur. Rapid assessment (e.g., cardiac catheterization) and intervention (e.g., valve repair or replacement) are critical for a positive outcome.
Clinical manifestations
Acute: Thready peripheral pulses and cool, clammy extremities
Chronic: Asymptomatic for years until development of some degree of left ventricular failure
Initial symptoms include
Weakness
Fatigue
Palpitations
Dyspnea that gradually progresses to orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema
Auscultatory findings of accentuated left ventricular filling leading to audible S3
Murmur is loud pansystolic or holosystolic murmur located at apex radiating to left axilla.
Patients with asymptomatic MR should be monitored carefully, and surgery (valve repair or replacement) should be considered before significant left ventricular failure or pulmonary hypertension develops.
Ischemic papillary muscle dysfunction
Infective endocarditis
Management of mitral regurgitation is the same as that for congestive heart failure
Usually, patients with mitral regurgitation benefit from afterload reduction (arterial dilation) by treatment with angiotensin-converting enzyme (ACE) inhibitors, such as captopril (Capoten), enalapril (Vasotec), lisinopril (Prinivil, Zestril), ramipril (Altace), or hydralazine (Apresoline).
Antibiotic prophylaxis therapy is instituted to prevent infectious endocarditis.
Once symptoms of heart failure develop, the patient needs to restrict his or her activity level.
Surgical intervention consists of mitral valvuloplasty (ie, surgical repair of the heart valve) or valve replacement.

23. Mitral Valve Prolapse
Mitral valve prolapse is usually an inherited connective tissue disorder resulting in enlargement of one or both of the mitral valve leaflets.
Infective endocarditis may cause perforation of a leaflet, or the scarring following the infection may cause retraction of the leaflets or chordae tendineae.

24. Aortic Valve Stenosis
Results from a previous rheumatic fever or fibrocalcific degeneration in older adults
Valve leaflets stiffen and retract, stenosis occurs
Obstruction of blood flow from left ventricle to aorta during systole

25. Aortic Valve Regurgitation
Caused by infective endocarditis, trauma, or aortic dissection
Retrograde blood flow from ascending aorta into LV during diastole=volume overload=hypertrophy, decreased contractility=pulmonary HTN & RVF
Acute AVR =Life threatening emergency
Chronic AVR= result of rheumatic heart disease, congenital disorders;

26. Tricuspid & Pulmonic Valve disease
Uncommon
Stenosis occurs more frequently than regurgitation
Increase in blood volume to RA and RV
RA enlargement & elevated systemic venous pressures

27. Collaborative Care of Valvular Heart Disease
Prevention
Anticoagulant therapy
Percutaneous Transluminal Balloon Valvuloplasty
Surgery
Valvulotomy (valve repair)
Prosthetic mechanical valves (valve replacement)
Prosthetic biologic valves (valve replacement)

28. Questions?
For more information and to post follow up comments or questions:
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29. References
Lewis, S., Heitkemper, M, & Dirksen, S. (2007). Medical Surgical Nursing, 7th Ed.. St. Louis: Mosby, Chapter 37.
Lewis, S., Heitkemper, M, & Dirksen, S. (2011). Medical Surgical Nursing, 8th Ed.. St. Louis: Mosby, Chapter 37.
National Heart Lung and Blood Institute. (2012). What is heart valve disease? Retrieved from topics/topics/hvd/
National Heart Lung and Blood Institute. (2012). What is endocarditis? Retrieved fromhttp:// topics/topics/endo/
Youtube.com. (2012). How the heart works animation video. Retrieved April 6, 2012 from &feature